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Questions and Answers
Which condition is NOT typically associated with pre-renal azotemia?
What is a key physical sign indicating pre-renal azotemia?
Which class of medications is recognized for potentially inducing pre-renal azotemia?
Which type of Acute Kidney Injury is characterized by intrinsic damage to the kidneys?
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What is an essential step in the evaluation of Acute Kidney Injury?
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What urine osmolality measurement is indicative of pre-renal acute kidney injury (AKI)?
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In what condition would you expect urine sodium levels to exceed 20 mmol/L?
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What finding is often associated with a poorer prognosis in acute kidney injury?
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What is the typical urine osmolality to serum osmolality ratio in acute tubular necrosis?
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Which of the following is NOT a typical finding in pre-renal acute kidney injury?
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What is a common cause of acute kidney injury (AKI) that requires careful monitoring?
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Which of the following physical signs is indicative of systemic vasculitis with glomerulonephritis?
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Which of the following symptoms would likely indicate ureteric obstruction?
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What function is primarily carried out by the glomeruli in the kidneys?
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The presence of proteinuria is most closely related to which of the following?
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In assessing tubular integrity, which test is less commonly performed compared to tests of glomerular function?
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Which test results would most likely provide insights into acid-base regulation of the kidneys?
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What is the primary focus when assessing renal function through urinalysis?
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What is the significance of a Neutrophil gelatinase-associated lipocalin (NGAL) level exceeding normal ranges shortly after injury?
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Which urinary index indicates a tubular injury when its value is greater than 14?
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Which of the following conditions would not lead to the increased expression of Kidney Injury Molecule 1 (KIM-1)?
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What defines Acute Kidney Injury (AKI) concerning serum creatinine levels according to KDIGO guidelines?
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Which statement about IL-18 is correct in the context of acute kidney injury?
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Which of the following is true regarding the protein L-FABP in the context of renal injury?
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What role does acid-base status play in the evaluation of pre-renal acute kidney injury (AKI)?
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In the evaluation of acute kidney injury, what would be a misleading indicator?
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Study Notes
Diagnostic Evaluation
- The clinical context, history, and physical examination can help determine the cause of AKI
Pre-Renal Azotemia
- Clinical Setting: Blood loss, Vomiting, Diarrhea, Glycosuria causing polyuria, Drugs
- Physical Signs: Orthostatic hypotension, Tachycardia, Reduced jugular venous pressure, Decreased skin turgor, and Dry mucous membranes
Intrinsic Renal
- History: Suggestive of progression from Pre-Renal AKI (Ischaemic Spectrum) Exposure to specific Nephrotoxins
- Drug Doses Must be adjusted for GFR- Idiosyncratic reactions may occur
- Signs: Palpable Purpura, Pulmonary Hemorrhage → Systemic Vasculitis with Glomerulonephritis, Livedo reticularis, and other signs of emboli to the legs → Athero-Embolic disease, Signs of limb ischemia may suggest rhabdomyolysis
Post-Renal AKI
- History: Prostatic disease, nephrolithiasis, or pelvic or para-aortic malignancy
- Symptoms: Ureteric Obstruction → Colicky flank pain radiating to the groin, Prostatic Disease → Nocturia, Urinary Frequency or Hesitancy, Bladder enlargement → Abdominal fullness and suprapubic pain
- Diagnosis: Requires radiologic investigations
Biochemical Tests of Renal Function
- Assessment of Renal function should start with examination of the Urine
- Simple observation still contributes to the investigation
- Observations must be made on a freshly voided sample
- Diseases affecting the kidneys can selectively damage glomerular or tubular function
- Isolated disorders of tubular function are relatively uncommon
- In Acute Kidney Injury, there is a loss of function of whole nephrons
- Tests of Glomerular function are invariably required
Principal Functions
- Glomeruli: Filter water, Filter Low Molecular Components, Retain High Molecular Components, Retain Cells
- Tubules: Reabsorption of Glucose, K, Na, Bicarbonate, Amino Acids, Reabsorption of Water → Urine concentration ability, Acid-Base Regulation
Assessment of Glomerular Integrity
- GFR or Equivalent Tests: Urea, Creatinine, Cystatin C
- Glomerular Filtration Barrier Integrity: Proteinuria, Haematuria (Red Blood Cells), Red Cell Casts
Assessment of Tubular Integrity
- Tests: Glycosuria, Amino Aciduria, Proximal Tubular Reabsorption Ability, Acid-Base Regulation, Renal Concentrating Ability → Osmolality
Urinalysis
- Volume: Reduction in urine output usually denotes more severe AKI and is associated with a poorer prognosis
- Oliguria: This is due to tubular injury and resultant inability to reabsorb sodium
- Osmolality: The urine concentrating ability of the kidney is dependent upon many factors, Adequate tubular function in multiple regions of the kidney is vital
- Pre-Renal AKI : Urine Osmolality > 500 mOsm/kg This is consistent with: an intact medullary gradient and elevated serum vasopressin levels causing water reabsorption resulting in concentrated urine
- Renal AKI : Urine Osmolality < 350 mOsm/kg Due to loss of concentrating ability
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Urine Osmolality: Serum Osmolality
- Pre-Renal AKI: Urine Osmo : Serum Osmo > 1.3
- ATN: Urine Osmo : Serum Osmo < 1.3
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Summary of Diagnostic Tests:
- Urine Microscopy: + Hyaline casts (Pre Renal), Muddy brown Coarse granular casts, free renal tubular cells (ATN)
- Spot Urine Na: < 20 mmol/L (Pre Renal) , > 20 mmol/L (ATN)
- FENa: 2 % (Pre Renal), > 3 % (ATN)
- Serum Urea: > 70 (Pre Renal), Usually “normal”
- Urine: Serum Osmolality > 1.3 (Pre Renal), <1.3 (ATN)
Novel Biomarkers
- Neutrophil gelatinase-associated lipocalin (NGAL):
- Protein expressed by neutrophils and epithelial cells
- The encoding gene is upregulated in the presence of renal ischemia, tubule injury, and nephrotoxicity. Measured in plasma and urine.
- Useful early predictor with prognostic value
- Kidney Injury Molecule 1 (KIM-1): Transmembrane protein, Abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins
- Other Biomarkers: IL-18 (Interleukin), Liver fatty acid–binding protein (L-FABP), Tissue inhibitor metalloproteinase inhibitor 2 (TIMP-2), Insulin growth factor– binding protein 7 (IGFBP7)
AKI Diagnosis (KDIGO)
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AKI is defined as any of the following:
- Increase in Serum Creatinine by >26.5 mol/l within 48 hours; or
- Increase in Serum Creatinine to >1.5 X baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume ↓ excretion of acids, Impaired H secretion & Regeneration of HCO3, Reduced ammoniagenesis
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Description
Test your understanding of diagnostics related to Acute Kidney Injury (AKI). This quiz covers the clinical context, physical examination signs, and the distinctions between pre-renal, intrinsic, and post-renal causes. Assess your knowledge and improve your clinical skills in nephrology.
